1. Field of the Invention
This invention relates to the field of neuroaudiological differential diagnosis of the auditory system using a correlation of a unique “bottom-up” and “top-down” evaluation paradigm. The process uses both psychophysical and electrophysiological data collection techniques to measure the effects evoked by a single manipulated stimulus on the entire auditory system from the cochlea to the cortex.
2. Description of the Related Art
Tinnitus is defined as a persistent ringing, buzzing, or similar noise distraction in a patient's sensory perception of sound. The patient “hears” the phenomenon in the absence of an actual sound stimulus. Efforts to qualify and quantify tinnitus for the purpose of obliterating its debilitating effects have been protracted and expansive. The driving force in dealing with tinnitus has been the audiological measurement of suspected related hearing loss and the manipulation of maskers or phase-dependant stimuli to attempt to cover or cancel the offending noise(s). Since most tinnitus is tonal (a constant ringing), the logic has been that if the frequency of the tone could be isolated then a specific masking complex could be developed to cover up the offending tone.
Early conventional wisdom suggested that tinnitus was largely of cochlear origin but several studies have been recently conducted that point to the central nervous system as the origin. Recent studies have employed positron-emission tomography (“PET”) to actually monitor cerebral blood flow (“CBF”) in the central auditory system to see if tinnitus possibly resulted from excessive spontaneous activity in the central auditory system. These studies reported CBF changes in the left temporal lobe for patients with right ear tinnitus, whereas bilateral temporal lobe activity occurred in response to a peripheral tonal stimulation in the right ear.
The same studies concluded that tinnitus is not of cochlear origin but rather originates within the central auditory system since tones evoked more CBF activity in tinnitus sufferers than in control subjects.
Other studies have suggested that tinnitus has many similarities with the symptoms of neurological disorders such as paresthesia and central neuropathic pain caused by functional changes in specific parts of the central nervous system. Since much more is known about pain than tinnitus, the same studies suggested that it is possible to use pain as an algorithm to the understanding of the pathophysiology of tinnitus.
Subjective tinnitus can accompany hearing loss associated with exposure to loud sounds or noise trauma, after administration of ototoxic drugs, as a co-occurrence with presbycusis, as a part of the Ménière's syndrome, and as part of vestibular Schwannoma (as well as many other conditions). It also occurs as part of total deafness. Tinnitus is known to be comorbid with posttraumatic stress disorder, traumatic brain injury, and other psychological sequalae.
Tinnitus may appear as a nearly pure tone, distorted sound, hissings, or thumping; it can be manifested as recruitment of sound (an abnormal increase in perceived loudness as a sound is intensified), phonophobia (fear of sounds) or in cases where acoustic reflexes are changed. Tinnitus can be perceived as an external noise on one side, an external noise on both sides, or a noise within the head. There is evidence that the pathophysiology of unilateral and bilateral tinnitus is different. There is considerable evidence that expression of neural plasticity plays a central role in the development of the abnormalities that cause many forms of chronic subjective tinnitus.
Expression of neural plasticity can change the balance between excitation and inhibition in the nervous system, promote hyperactivity, and it can cause reorganization of specific parts of the nervous system or redirection of information to parts of the nervous system not normally involved in processing of sounds (non-classical or extralemniscal pathways). Since there are many kinds of subjective tinnitus, a search for a (single) cure for tinnitus is rather fruitless if not futile. Testing of new treatments is also hampered by the fact that it is not possible to distinguish between different forms of tinnitus for which different treatments may be effective.
Still other studies have linked tinnitus to central nervous system neurodegeneration. They used nuclear medicine brain imaging (i.e. PET) to study subjects with Alzheimer's disease and challenged the time-honored sensorineural view of subjective tinnitus and its subsequent clinical application for treatment. They concluded that subjective tinnitus occurs as the result of a central disorder.
Work has been done to explore the use of event related potentials (ERP) to study the pathogenesis of tinnitus and to attempt to correlate psychophysiological and neurophysiologic tinnitus and to better understand tinnitus decompensation. These studies used top-down event related potentials (“ERP”) methodology. Other studies also used auditory evoked cortical potentials (“AECP”) in the diagnosis of attention deficit disorder, etc and for studying tinnitus decompensation. A model of neural correlates to auditory attention reflected in AECPs using corticothalamic feedback dynamics was suggested. The model applies a multiscale of evoked potentials to the hearing path and discusses neuro functionality in terms of corticothalamic feedback loops related to focal and non-focal attention and objective tinnitus decompensation measure. Magnetic resonance spectroscopy (“MRS”) to identify unique in vivo metabolic and neurobiochemical biomarkers associated with tinnitus in specific regions of the central nervous system (“CNS”).
The emerging view is that treating the symptom is not effective and given the number of disorders comorbid with tinnitus a top-down analysis of the origin of tinnitus in conjunction with other neurological entities is needed. Patients who suffer from a variety of neurological disorders report tinnitus as an accompanying symptom. These disorders includes things such as central auditory processing disorders (“CAPD”), attention deficit hyperactivity disorder (“ADHD”), autism, dyslexia, learning disabilities, etc.
The proposed inventive method therefore focuses on the mapping of neurological disorders along the auditory pathways using dichotic stimuli in an array of psychophysical paradigm for tracking hearing defects along the total auditory pathway from the cochlea to the central auditory processing areas (bottom-up) verified by a top-down objective procedure using the very same stimuli.
Tinnitus results as a symptom of many primary auditory disorders rather than a unique pathology unto itself. In some cases treating the pathology will alleviate the tinnitus. In other cases the site of lesion of the primary disorder is unknown leaving the tinnitus as a phantom somewhere within the auditory network.
The present method uses a unique top-down neuroaudiological stimulus apparatus and procedures to place electric “markers” along the dichotic auditory pathways that can then be used in a bottom-up psychophysical paradigm to find those same “markers”—thereby assisting in the differential diagnosis of auditory problems from the cochlea to the cortex.
FIG. 1 is a conventional diagram of the main neural stations where “markers” can be placed using auditory evoked potentials (“AEP”) techniques such as the well-established diagnostic procedure of auditory brainstem response (“ABR”). The use of a top-down CAPD event marker for a click stimulus in but one ear (monaural) is shown in FIG. 1.
The reader should note that ABR is an objective electrophysiological process that requires no psychophysical behavioral response from the patient. A monaural click stimulus delivered to either ear is shown as it passes bottom-up through the auditory pathways. The numbers shown on the waveform (a) reflect the marker point of emergence of neuroelectricity for each wave.
When binaural stimuli are presented, the interactive crossover at the marker points are neurologically modified to provide the brain with information far beyond monaural stimulation. One added set of information in the dichotic stimulus (stimulus to both ears) is the perceived location of the source of the sound. Each side of the brain processes information from the opposite side of the auditory system with the brainstem serving as the primary switchboard.
FIG. 1 represents the neural transmission of a monaural stimulus (a stimulus to only one ear). Note that a majority of the energy is sent to the opposite side of the brain from the stimulus. However, some neural tracts continue along the ipsilateral side of the neural pathways. When a binaural stimulus is simultaneously presented to both ears (diotic stimuli)—and each side of the auditory processing system is individually neurophysiologically recorded—the results appear as shown in FIG. 2.
FIG. 2 shows a plan view looking down on the top of a patient's head. Ground electrode 14 is placed on the midline. Left electrode 16 is placed proximate the patient's left ear. Right electrode 18 is placed proximate the patient's right ear. Left ear phone 20 delivers a stimulus to the left ear and right ear phone 22 delivers a stimulus to the right ear.
FIG. 2-a is a typical monaural waveform resulting from a stimulus applied to only one ear. FIG. 2-b shows data obtained from a three electrode montage (two measuring electrodes and one ground reference electrode) when a diotic stimulus (identical stimulus applied to each ear at exactly the same time) is applied.
A three electrode montage is rather simple and is presented only to convey the concept. The use of a more standard 20 electrode EEG montage will further identify unique dichotic cortical markers using brain electric activity mapping (“BEAM”) with the same stimulus used in FIG. 2-b. 
The reader will observe that the two waves shown in FIG. 2-b do not overlie each other. The brain map will reflect the lead/lag or lag/lead perceived position of the stimulus as a shift in the voltage of the electrodes along the cortex. This is sometimes referred to as a virtual image analysis (“VIA”). VIA refers to the brain's ability to analyze sound stimuli and create a virtual image of the location of the spatial location of the source of the sound. As will be explained in detail subsequently, a perfectly symmetric sound stimulus as shown in FIG. 2 is not perceived as a “centered” sound by the brain.
A “VIA setting” refers to the lead or lag of a stimulus applied to one ear versus the other. This lead or lag relationship alters the brain's perception as to the location of the source of the sound.
Brain electric activity mapping (“BEAM”) maps the instantaneous electrical differential between a reference electrode (ground) and the balance of the electrode array mapped in different colors representing the relative voltages. FIG. 3 shows a typical brain map for two different VIA settings (one on FIG. 3-a and one in FIG. 3-b).
In keeping with the convention for patent drawings the images of FIG. 3 are not presented in color. However, it is important for the reader to understand that they are conventionally presented in color to a user of the inventive method.
FIG. 4 shows normal data for a right handed subject (FIG. 3-a shows the BEAM maps for the same stimulus). The reader will observe that right stimulus 26 is delivered through right earphone 22 slightly before left stimulus 24 is delivered through left ear phone 20. The auditory brainstem response waves 28 (“ABR waves”) are closely matched from left to right (They lie closely over each other).
Changing the VIA setting (the lead-lag of the right versus left stimulus) will change the ABR wave configuration and the BEAM map. Changing the VIA lead-lag from left to right will “reverse” the ABR waves and the BEAM map depending on brain dominance (whether the patient is left brain dominant or right brain dominant). The VIA arrangement is reflected in an overall shift of the ABR assemblage with the dominant hemisphere waveforms appearing at an earlier time.
FIG. 5 shows the effect of changing the VIA setting on the resulting ABR waves. (See FIG. 5). Here the transformation that takes place as a result of lead/lag or lead/lag dichotic configuration is shown. As the VIA is increased the individual waveforms shift in time to a greater or lesser number. Likewise the right and left waveforms shift together but take on different “shapes” depending on the VIA differential. In addition the entire assemblage shifts in time linked to hemispheric dominance.
Psychophysical Auditory Phenomenon: (Normal Auditory Processing)
The brain is not unilaterally equal to auditory stimulation. This natural brain dominance accounts for sound localization (spatially locating the source of the sound) and is an important component in central auditory processing. Factored into this is the fact that the balance mechanism is part of the auditory system that may contribute to tinnitus. There is an optimum overlay pattern (of the left and right ABR waves) where the natural hemispheric dominance is tuned to the point where sound is localized to the center of the head (The patient perceives the sound as coming from the center of the head). The human ear can psychophysically detect a time change of as little as 64 usec using a 100 usec, 60 dB square wave as a dichotic stimulus. FIG. 4 shows the ABR correlate of the behavioral position of zero. As can be seen the actual dichotic neurological midline position is off center (meaning that the timing of the stimulus transmitted to the two ears must be varied in order to place the left and right ABR waves on top of each other).
FIG. 6 also shows this phenomenon. Purely diotic stimuli (in which a stimulus is presented simultaneously to each ear) produces a perception of the sound being off center to one side or the other (depending upon whether the individual is right brain dominant or left brain dominant).
Dichotic Listening
Historically Dichotic listening has been described as the simultaneous presentation of different stimuli to both ears. It appears that in dichotic stimulation, contralateral pathways from the ears to the opposite hemispheres suppress the ipsilateral pathways from the ears to the same hemispheres. In most right-handed persons there is a right ear advantage because the path from the right ear goes contralaterally to the dominant left hemisphere. In behavioral psychophysical procedures this process is reflected as a positional location about the head. If the time between two stimuli is varied in microseconds as lead/lag/or lag/lead the stimulus pair is reported to be moving from place to place about the head. Under earphones this positional location moves from being into both ears at larger time differentials and moves toward the center of the head as the time is lessened to ultimately focus at midline at approximately 100 microseconds lead/lag for normal right dominant subjects and vice versa for left dominant subjects. FIG. 5 shows this relationship for neurological studies and FIG. 6 show the psychophysical positioning (the term “psychophysical” meaning the user's perception of position). These responses are part of the bottom-up paradigm.
Bottom Up Diagnostic Processes
Tone decay, tinnitus and recruitment of loudness are three critical diagnostic indicators in the differential diagnosis of hearing disorders. Recruitment is a diagnostic indicator of cochlear pathology and is manifested as an abnormal growth of loudness. Tone decay occurs when a continuous tone appears to diminish as the tone is continued without change over a fixed period of time and is considered as an indicator of retrocochlear pathology. Tinnitus is discussed in detail later.
In the late 1940's, a “New Audiometer” was described that used the classical psychophysical method of adjustment to present constantly changing tones to a subject who alternately adjusted the intensity of those tones from the just noticeable difference (JND) to the just not noticeable difference (JNND) thereby crossing absolute threshold numerous times. This work resulted in the formulation of the classic Bekesy Audiograms that were later standardized into the four basic patterns. FIG. 7 shows Bekesy's own original classification (1960) of audiograms obtained on his New Audiometer. FIG. 7 shows a single continuous tracing to plot a conductive hearing loss (top), a sensorineural hearing loss (middle) and one with tinnitus (bottom).
Bekesy suggested that recruitment of loudness is demonstrated in the narrowing of the tracings following a pattern of normal excursions and retro-cochlear lesions are displayed as rapid tone decay. This work was extended by others to a continuous tone to an interrupted tone so as to reveal both tone decay and recruitment. Examples of Jerger's original classification of the Bekesy audiograms are shown in FIG. 8 (Type I, Normal; Type II, Cochlear; Type III and Type IV Retrocochlear).
The minimal auditory intensity differential (“MAID”) used a single on-going stimulus to derive similar results as gained by the Bekesy audiograms. FIG. 9 shows the design of a MAID-type signal. If a constant intensity/frequency pure tone is varied in amplitude four times/sec with no rise-fall envelope (yet with no electrical switching transient), the change in intensity is perceived by a listener as (1) a difference limen (“difference limen” being synonymous with JND or “just noticeable difference”) to intensity and (2) a four times per second click. The resultant perception is an ongoing two component stimulus which can be psychophysically manipulated to look at the relationship of a continuous to interrupted tone (see Bekesy Type III) while at the same time looking at the click perception threshold which yields recruitment data (see Bekesy Type II and IV). In retrocochlear lesions the click perception threshold is normal and the carrier puretone fades away leaving the patient only perceiving the four times per second click. Hence the MAID-type signal provides a psychophysical methodology for the determination of both cochlear and retrocochlear hearing disorders with a single stimulus. The perception of that change is dependant on the presence of the site of lesion and the degree of pathology. The MAID functions primarily as a cochlear/retrocochlear differential test.
The MAID-type signal can be made dichotic by presenting it to each ear independently. The right ear wave was kept constant and the left ear wave was “slid” (phase shifted) back and forth occurring either in a lead or a lag position. The perceived behavioral placement of the source of the sound on the head was dependant on the time of the lead/lag or lag/lead.
By changing the onset times of the signal to one ear with respect to the signal for the other ear a virtual image (“VIA”) is established in the user's perception (the location of the sound source seems to change). If wave B is adjusted in time-steps from about 100 μusec to 2 msec the sound source appears to move from one ear, across the mid plane, and then to the opposite ear with the midpoint being perceived as being off-center.
Because of the complexity of the MAID stimulus a single click of 100 μsec duration (standard ABR stimulus) was delayed in the previously described lead/lag//lag/lead (VIA) version for electrophysiological application. (The new version of the stimulus presented in the inventive method returns to the roots of the MAID and changes the stimulus for electrophysiological use by removing only the puretone carrier).
FIG. 11 is a schematic of the VIA stimulus. The MAID envelope with only the removal of the puretone serves the same purpose as the VIA.
FIG. 12 is a diagram of the revised stimulus (The MAID envelope with only the removal of the puretone). This change generates a new stimulus only one component away from the MAID-type signal and becomes more reliable in the differential diagnosis paradigm. Furthermore the change in intensity (“ΔI”) is situated onto a constant ongoing baseline stimulus rather than silence and allows for a more subtle change at the stimulus point.
Children: Neurological Disorders and Tinnitus
Any mention of central dysfunction should necessarily move into a discussion of central auditory processing disorders (CAPD) and, more specifically, labeled disorders such as autism and traumatic brain injury (“TBI”) in children. Children are seldom included in the discussion of tinnitus even though they do suffer the disorder but, more importantly, they comprise the major population of sufferers of central neurological disorders. Tinnitus is present in child subjects with hearing loss and central sensory perception and emotional problems. When exploring the risk factors in children, a relationship was found between tinnitus and a history of noise exposure, motion sickness, hyperacusis and hearing loss. The coexistence of tinnitus and hyperacousis in these studies introduces the possibility that tinnitus might be a factor in disorders such autism and TBI.
Hyperacusis has been found in an autistic group when compared to controls. The use of biomarkers of brain injury has also been discussed in the field of TBI. TBI is a leading cause of emergency department care with seemingly minor head trauma account for approximately one-half of children with documented TBIs. Despite the frequency and importance of childhood minor head trauma, there exists no highly accurate, reliable and validated clinical scoring system or prediction rule for assessing risk of TBI among those with minor head trauma.
Hearing loss has four major diagnostic categories. The first two (peripheral) have clearly defined medical diagnostic indicators: (1) Conductive, due to obstruction or infection in the outer or middle ear and is identified via otoscopy, audiograms (air and bone conduction) and tympanometry; (2) sensorineural that occurs within the neural transduction system of the cochlea (including the semicircular canals) and is fairly accurately defined by way of audiograms, speech discrimination scores, recruitment, ENG and tone decay to a lesser degree (3) retrocochlear and brainstem that occurs within the VIIIth cranial nerve to the auditory cortex and is defined by tone decay testing, audiometry, ENG (etc), ABR and (4) Central occurring in the vestibulocerebellum that controls balance (input from the inner ears), eye movement and central auditory processing.
The third and fourth diagnostic categories comprise the central processing system which serves as an elaborate “switch board” that routes neural signals via the brainstem to ipsi/contralateral positions on the cortex and cerebellum. One common element of all of these hearing disorders is tinnitus. Given this coincidence of pathology and tinnitus, the presence of tinnitus in children with hearing disorders (conductive, cochlear, retrocochlear, or central) means that the probability of tinnitus being a disruptive development element is high.
Tinnitus and Auditory Processing
Measurement efforts in tinnitus have spanned the spectrum of diagnostic instruments and methods with psychoacoustics being the most favored technique even though some have suggested that the more commonly used behavioral information of pitch, loudness, maskability, and residual inhibition do not yield consistent relationship to the severity or perceived loudness of tinnitus. A search for psychophysical tools lead to the methods of bracketing, limits, and adjustment for the measurement of pitch in the ear ipsilateral to the tinnitus. Some have used strict psychoacoustics methodology to explore the reaction times of normal hearing subjects with and without tinnitus. Of importance to the present study is their finding that tinnitus sufferers had shorter reaction times at sensation levels near threshold than did normal patients—with no significant differences between groups at sound stimuli in the suprathreshold intensity range. Several studies have noted the tendency for near threshold activities to be more productive than louder ones.
Little quantitative measurement of tinnitus was possible before the development of the electric audiometer. Since then many attempts have been made to simulate the phenomenon. Frequency and masking measurements were first described in 1931 along with techniques involving loudness balance, free-field matching and taped sound effects. It has been suggested that a music synthesizer might be a more appropriate tool for tinnitus matching since the audiometer is limited in frequency selection.
One approach used a patient tracking psychophysical method using continuous sweeping frequencies (20 to 20 kHz) and determined this methodology to be much more productive than standard methods of audiometry.
Another study compared the hearing sensitivity and psychological profile of young subjects with tinnitus and normal hearing. The test procedures used pure-tones (including high frequencies), notched-noise, auditory-brainstem responses, and evoked otoacoustic emissions. Psychophysical and brainstem tests were comparable to those of normal hearing subjects without tinnitus. Otoacoustic emissions were “worse” in ears of tinnitus subjects and neurotic personality traits were stronger in the tinnitus subjects.
A psychometric numeric rating scale has been used to detail the different perceptual components of tinnitus; i.e. auditory sensations which are perceived in the absence of a corresponding external acoustic stimulus. Some such studies measured pitch (in 0.2% steps) and loudness (in 2 dB steps) of tinnitus using a forced-choice double-staircase procedure and found that the difference limen (JND) of pitch and loudness were not significantly different from that of the same measurements made to comparable external stimuli.
The most studied area of tinnitus has to do with masking the offending phenomenon. Early masking efforts employed psychoacoustics. More recent psychoacoustic studies have looked into central involvement as apposed to the severity of hearing loss. On masking technique used low-level ultrasound in an attempt to inhibit tinnitus. Another technique evaluated various electrical stimuli via the mastoid processes for their ability to suppress or relieve severe tinnitus.
Pulsed electromagnetic stimulation applied on the mastoid bone has offered little improvement. Experiments using lasers have also shown no significant results. Other experiments used two separate audio frequency generators to shift the phase of the second generator in relationship to the first generator (set at the audiometrically-determined frequency-matched monofrequency of the tinnitus) by 180 degrees so that a third sound was delivered simultaneously to both ears. This theory supposed that cancellation would result but in reality a third multi-frequency masking stimulus was produced that would randomly match the monofrequency tinnitus.
The past 15 years have seen the most change in tinnitus evaluation and management. The very active classical psychophysics research in audition of the 1930's set the stage for the use and understanding of psychoacoustics techniques. Studies of tinnitus masking and residual inhibition exploded in the 1970's, leading to the therapeutic use of masking and an increase in research of psychoacoustic measurement with pitch, loudness, maskability, and residual inhibition emerging as foci.
The ideal solution would be to cancel out tinnitus without introducing external noise. The next best solution would be to reduce or cancel the tinnitus as well as the intensity of the masking stimulus. The present invention presents a psychoacoustics technique that either totally cancels tinnitus or replaces it with a barely discernable external noise of lesser volume and no pitch characteristics. The approach takes advantage of several well known, and some lesser known, auditory neurological patterns of change that occur in both normal and pathological ears including, but not limited to (1) binaural summation; (2) temporal asymmetry; (3) “recruitment” and tone decay; and (4) dichotic brain dominance.